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Car indoor air pollution - analysis of potential sources
Journal of Occupational Medicine and Toxicology 2011, 6:33 doi:10.1186/1745-6673-6-33
Daniel Mueller ()
Doris Klingelhoefer ()
Stefanie Uibel ()
David A Groneberg ()
ISSN 1745-6673
Article type Review
Submission date 2 August 2011
Acceptance date 16 December 2011
Publication date 16 December 2011
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1
Car indoor air pollution – analysis of potential sources

Daniel Müller
1
, Doris Klingelhöfer
1
, Stefanie Uibel

1
,

David A. Groneberg
1

1
Institute of Occupational, Social and Environmental Medicine, Goethe-University,
Frankfurt, Germany

Email
Daniel Müller - , Doris Klingelhöfer -
, Stefanie Uibel - ,
David A. Groneberg -



Corresponding author: Daniel Müller –

2
Abstract
The population of industrialized countries such as the United States or of countries
from the European Union spends approximately more than one hour each day in
vehicles. In this respect, numerous studies have so far addressed outdoor air
pollution that arises from traffic. By contrast, only little is known about indoor air
quality in vehicles and influences by non-vehicle sources.
Therefore the present article aims to summarize recent studies that address i.e.
particulate matter exposure. It can be stated that although there is a large amount of
data present for outdoor air pollution, research in the area of indoor air quality in
vehicles is still limited. Especially, knowledge on non-vehicular sources is missing. In

this respect, an understanding of the effects and interactions of i.e. tobacco smoke
under realistic automobile conditions should be achieved in future.



3
Introduction
Air quality plays an important role in occupational and environmental medicine and
many airborne factor negatively influence human health [1-6]. This review
summarizes recent data on car indoor air quality published by research groups all
over the world. It also refers to formerly summarized established knowledge
concerning air pollution. Air pollution is the emission of toxic elements into the
atmosphere by natural or anthropogenic sources. These sources can be further
differentiated into either mobile or stationary sources. Anthropogenic air pollution is
often summarized as being mainly related to motorized street traffic (especially
exhaust gases and tire abrasion). Whereas other sources including the burning of
fuels, and larger factory emissions are also very important, public debate usually
addresses car emissions.
The World Health Organization (WHO) estimates 2.4 million fatalities due to air
pollution every year. Since the breathing of polluted air can have severe health
effects such as asthma, COPD or increased cardiovascular risks, most countries
have strengthened laws to control the air quality and mainly focus on emissions from
automobiles.
In contrast to the amount of research that is currently conducted in the field of health
effects, only little is known on specific exposure situations due to external sources
which are often present in the indoor environment of a car but not related to the car
emissions. The studies addressed a number of vehicular or non-vehicular sources
(Fig. 1).

Particulate matter components

One general study assessed the exposure to fine airborne particulate matter (PM
2.5
)
in closed vehicles [7]. It was reported that this may be associated

with cardiovascular

4
events and mortality in older and cardiac

patients. Potential physiologic effects of in-
vehicle, roadside,

and ambient PM
2.5
were investigated in young, healthy, non-
smoking,

male North Carolina Highway Patrol troopers. Nine troopers (age

23 to 30)
were monitored on 4 successive days while working

a 3 P.M. to midnight shift. Each
patrol car was equipped with

air-quality monitors. Blood was drawn 14 hours after
each shift,

and ambulatory monitors recorded the electrocardiogram throughout

the
shift and until the next morning [7]. Data were analyzed using

mixed models. In-
vehicle PM
2.5
(average of 24 µg/m
3
) was

associated with decreased lymphocytes (–
11% per 10 µg/m
3
)

and increased red blood cell indices (1% mean corpuscular
volume),

neutrophils (6%), C-reactive protein (32%), von Willebrand factor

(12%),
next-morning heart beat cycle length (6%), next-morning

heart rate variability
parameters, and ectopic beats throughout

the recording (20%) [7]. Controlling for
potential confounders had

little impact on the effect estimates. The associations of
these

health endpoints with ambient and roadside PM
2.5
were smaller

and less
significant. The observations in these healthy young

men suggest that in-vehicle
exposure to PM
2.5
may cause pathophysiologic

changes that involve inflammation,
coagulation, and cardiac

rhythm [7].
A second study by Riedecker et al. assessed if the exposure to fine particulate matter
(PM2.5) from traffic affects heart-rate variability, thrombosis, and inflammation [8].
This work was a reanalysis and investigated components potentially contributing to
such effects in non-smoking healthy male North Carolina highway patrol troopers.
The authors studies nine officers four times during their late shift. PM2.5, its
elemental composition, and gaseous copollutants were measured inside patrol cars
[8]. Components correlating to PM2.5 were compared by Riedecker et al. to cardiac
and blood parameters measured 10 and 15 h, respectively, after each shift. The
study demonstrated that components that were associated with health endpoints

5

independently from PM2.5 were von Willebrand Factor [vWF], calcium (increased uric
acid and decreased protein C), chromium (increased white blood cell count and
interleukin 6), aldehydes (increased vWF, mean cycle length of normal R-R intervals
[MCL], and heart-rate variability parameter pNN50), copper (increased blood urea
nitrogen and MCL; decreased plasminogen activator inhibitor 1), and sulfur
(increased ventricular ectopic beats) [8].
The changes that were observed in this reanalysis were consistent with effects
reported earlier for PM2.5 from speed-change traffic (characterized by copper, sulfur,
and aldehydes) and from soil (with calcium) [7]. However, the associations of
chromium with inflammation markers were not found before for traffic particles. The
authors concluded that aldehydes, calcium, copper, sulfur, and chromium or
compounds containing these elements seem to directly contribute to the inflammatory
and cardiac response to PM2.5 from traffic in the investigated patrol troopers.
Interestingly, it was not studied whether other PM2.5 sources that frequently occur in
cars such as cigarette smoke have effects at this magnitude.
To understand the dynamics of particulate matter inside train coaches and public
cars, an investigation was carried out during 2004-2006 by Nasir and Colbeck [9].
They demonstrate that for air-conditioned rail coaches, during peak journey times,
the mean concentrations of PM10, PM2.5 and PM1 were 44 µg/m3, 14 µg/m3 and 12
µg/m3, respectively [9]. They also reported that the levels fell by more than half (21
µg/m3, 6 µg/m3, and 4 µg/m3) for the same size fractions, on the same route, during
the off-peak journeys [9]. Also, non-air-conditioned coaches were assessed and it
was found that the PM10 concentrations of up to 95 µg/m3 were observed during
both peak and off-peak journeys. By contrast, concentrations of PM2.5 and PM1
were 30 µg/m3 and 12 µg/m3 in peak journeys in comparison to 14 µg/m3 and 6

6
µg/m3 during off-peak journeys [9]. The authors studied particulate air pollution in
transport micro-environments over a period of four months and within this period, the
concentrations of PM10, PM2.5 and PM1 in car journeys were generally similar

during both morning and evening journeys with average values of 21 µg/m3 for
PM10, 9 µg/m3 for PM2.5 and 6 µg/m3 for PM1 [9]. However, they also reported that
during October the average concentration of PM10 was 31 µg/m3. Interestingly, an
analysis of nearby fixed monitoring sites for both PM10 and PM2.5 showed an
episode of high particulate pollution over southern England during one week of
October. There was no statistically significant difference between particulate matter
levels for morning and evening car journeys. A statistically significant correlation was
present between morning and evening PM10 (0.45), PM2.5 (0.39) and PM1 (0.46)
[9]. The study also showed a statistically significant difference for peak and off-peak
levels of PM10, PM2.5 and PM1 in air-conditioned train coaches. On the other hand,
in non air-conditioned coaches a significant difference was documented only for
PM2.5 and PM1 [9].
Next to PM10 and PM2.5 focussed studies, also ultrafine particles (UFP) have been
assessed. In this respect, Liu and colleagues have aimed to quantify exposure to
UFP because of second hand smoke (SHS) and to investigate the interaction
between pollutants from SHS and vehicular emissions [10]. They measured the
number concentration and size distribution of UFP and other air pollutants such as
CO, CO2 and PM2.5 inside a moving vehicle under five different ventilation
conditions [10]. The vehicle was moved on an interstate freeway with a speed limit of
60 mph and on an urban roadway with a speed limit of 30 mph. It was shown that in
a typical 30-min commute on urban roadways, the SHS of one cigarette led to a
approximately 10 times increased amount of UFP and 120 times increased amount of

7
PM2.5 in comparison to ambient air [10]. The study indicated that window opening is
an effective method for decreasing pollutant exposures on most urban roadways. By
contrast some road conditions such as tunnels or crowded freeways with a high
proportion of diesel trucks do not allow window opening to be a safe method to
decrease UFP levels significantly. In summary, it can be concluded that high
ventilation rates may effectively reduce UFPs inside moving vehicles in some road

and driving conditions [10].
In parallel, Knibbs et al. assessed on-road and in-vehicle ultrafine (<100 nm) particle
(UFP) concentrations for five different passenger vehicles in an tunnel [11]. They
comprised an age range of 18 years. They study encompassed a range of different
ventilation settings which were assessed during more than 300 car trips through road
tunnel of 4 km in Sydney, Australia [11]. The study quantified the outdoor air flow
rates on open roads using tracer gas techniques. It was found that a significant
variability in tunnel trip average median in-cabin/on-road (I/O) UFP ratios is present
with 0.08 to approximately 1.0. A positive linear relationship was present between
outdoor air flow rate and I/O ratio, with the former accounting for a substantial
proportion of variation in the latter (R(2) = 0.81). Interestingly, UFP levels recorded
in-cabin during tunnel travel were found to be significantly higher than those reported
by comparable studies performed on open roadways [11]. Summarizing the data of
this study by Knibbs et al. it may be assumed that in-cabin UFP exposures incurred
during tunnel travel may contribute significantly to daily exposure under certain
conditions. It can also be stated that UFP exposure of automobile occupants appears
strongly to be related to the ventilation setting and the vehicle type [11].



8
Endotoxin and β-(1,3)-glucan
A recent study by Wu et al. addressed endotoxin and β-(1,3)-glucan levels in
automobiles [12]. This Taiwanese group from the Changhua Christian Hospital,
Changhua City, Taiwan postulated that exposure to bacterial endotoxin and fungal β-
(1,3)-glucan may also occur in the car indoor environment and can induce major
respiratory symptoms. It is known that cars are an exposure source of allergens but it
is not specifically known if, and how much exposure there is to fungal β-(1,3)-glucan
and endotoxin. Therefore the objective of the project was to assess whether
automobiles are a potential source of exposure to these products. Wu et al sampled

dust from the passenger seats of 40 cars [12]. A specific Limulus amoebocyte kinetic
assays was used to measure endotoxin and β-(1,3)-glucan, respectively. The authors
reported that endotoxin and β-(1,3)-glucan were detected in all samples ranging from
19.9-247.0 EU/mg and 1.6-59.8 µg/g, respectively. Significant differences in
endotoxin levels between automobiles of smokers and non-smokers were not found,
but β-(1,3)-glucan levels were about two-fold higher in the automobiles of non-
smokers [12]. It was concluded that endotoxin and β-(1,3)-glucan exposure in
automobiles at levels found in this study may be of importance for asthmatics [12].

Brominated flame retardants
Further substances that may occur in cars are polybrominated diphenyl ethers
(PBDEs), hexabromocyclododecanes (HBCDs), and tetrabromobiphenol-A (TBBP-
A). A recent project assessed these chemicals in dust from passenger cabins and
trunks of 14 UK cars [13]. It was reported that concentrations in cabin dust of HBCDs,
TBBP-A, and BDEs 47, 85, 99, 100, 153, 154, 183, 196, 197, 202, 203, 206, 207,
208, and 209 exceeded significantly (p<0.05) those in trunk dust. The authors

9
concluded that sampling cabin dust appears to provide a more accurate indicator of
human exposure via car dust ingestion than trunk dust [13]. Elevated cabin
concentrations are consistent with greater in-cabin use of brominated flame
retardants (BFRs). In five cars, while no significant differences (p>0.05) in
concentrations of HBCDs and most PBDEs were detected in dust sampled from four
different seating areas; concentrations of TBBP-A and of PBDEs 154, 206, 207, 208,
and 209 were significantly higher (p<0.05) in dust sampled in the front seats of the
cars [13]. Possible photodebromination of BDE-209 was indicated by significantly
higher (p<0.05) concentrations of BDE-202 in cabin dust. The authors also report that
in-vehicle exposure via dust ingestion to PBDEs, HBCDs and TBBP-A exceeded that
via inhalation [13]. Comparison with overall exposure via diet, dust ingestion, and
inhalation shows while in-vehicle exposure is a minor contributor to overall exposure

to BDE-99, ΣHBCDs, and TBBP-A, it is a significant pathway for BDE-209 [13].
Aromatic hydrocarbons
Next to particulate matter, other noxious compounds including aromatic
hydrocarbons, as well as aliphatic hydrocarbons, may play a role in indoor air quality.
They diffuse from interior materials in car cabins [14]. In a recent study, seven
selected aromatic hydrocarbons were assessed concerning their inhalation
toxicokinetics in rats. In brief, amounts of these substances were injected into a
closed chamber system containing one rat, and concentration changes in the
chamber were examined. Afterwards, toxicokinetics of the substances were analysed
on the basis of the concentration-time course using a nonlinear compartment model
[14]. Furthermore, the amounts absorbed in humans at actual concentrations in car
cabins without ventilation were extrapolated from the results obtained from rats. In
specific, the absorbed amounts estimated for a driver during a 2 h drive were as

10
follows per 60 kg of human body weight: 30 µg for toluene, 10 µg for ethylbenzene, 6
µg for o-xylene, 8 µg for m-xylene, 9 µg for p-xylene, 11 µg for styrene and 27 µg for
1,2,4-trimethylbenzene. Concomitantly, in a cabin in which air pollution was marked,
the absorbed amount of styrene (654 µg for 2 h in a cabin with an interior maximum
concentration of 675 µg/m3) was estimated to be significantly higher than those of
other substances [14]. This amount (654 µg) was approximately 1.5 times the
tolerable daily intake of styrene (7.7 µg/kg per day) recommended by the World
Health Organization [14].

Volatile organic compounds in car showrooms
Next to exposure inside vehicle, also car dealer showrooms may be places in which
occupants may be exposed to emissions from the exhibited vehicles [15]. In order to
identify and quantify the main organic compounds present in car dealer showrooms,
a total of 19 volatile organic compounds (aromatic compounds, aldehydes and
terpenes) were investigated and quantified in showrooms [15]. Also, the levels of the

same chemicals were measured in the private houses of the car vendors for
comparative purposes. The authors used passive samplers over a consecutive time
period of 5 days and reported that the concentrations in the showrooms were on
average 12 times higher than the ambient concentration around the showrooms and
10 times higher than the concentrations measured in the private houses. Interestingly
benzene concentrations inside the showrooms ranged from 11 to 93.2 µg/m3. It was
found that the personal exposure concentrations of the vendors reached time-
weighted levels up to 57.3 µg/m3 with minimum values around 10 µg/m3. Overall,
this study indicated that work place emissions contribute to a significant proportion of

11
a vendors' overall exposure load [15]. It can be concluded that high concentrations of
some volatile organic compounds (VOCs) that were recorded here, point to the
importance of occupational safety guidelines for car vendors [15].
Earlier, these authors analysed the presence of selected VOCs including aromatic,
aliphatic compounds and low molecular weight carbonyls, and a target set of
phthalates in the interior of 23 used private cars during the summer and winter [16].
They reported that VOC concentrations often exceeded levels typically found in
residential indoor air, e.g. benzene concentrations reached values of up to 149.1
µg/m3 [16]. Interestingly, overall concentrations were 40% higher in summer, with
temperatures inside the cars reaching up to 70 degrees C. The most frequently
detected phthalates were di-n-butyl-phthalate and bis-(2-ethylhexyl) phthalate in
concentrations ranging from 196 to 3656 ng /m3 [16].

Microbiological air quality and air conditioning systems
Concerning microbiological air quality and air conditioning systems, Vonberg et al.
assessed the impact of air conditioning systems in cars on the number of particles
and microorganisms inside vehicles recently [17]. For this purpose, over a time
period of 30 months, the quality of air was investigated in three different types of cars
which were equipped with an air conditioning system. Different operation modes

using fresh air from outside the car as well as circulating air from inside the car were
assessed and the total number of microorganisms and mold spores were analysed
using impaction in a high flow air sampler [17]. Also particles of 0.5 to 5.0 µm
diameter were analysed. In total, 32 occasions of sampling were performed and it
was shown that the concentration of microorganisms outside the cars was always
higher than it was inside the vehicles [17]. A few minutes after starting the air

12
conditioning system in the cars, it was found that the total number of microorganisms
was reduced by 81.7%. Similarly, the number of mold spores decreased by 83.3%
[17]. The number of particles was found to be reduced by 87.8%. Interestingly, the
authors did not find significant differences between fresh air vs. circulating air
conditioning systems or the types of cars. It may be suggested that the use of the car
air conditioning system can improve certain parameters of indoor air quality [17].

Residual tobacco smoke in used cars
Fortmann et al. recently focussed on residual tobacco smoke pollution (TSP) in cars
which is caused by frequently smoking cigarettes in a car's microenvironment [18].
They applied surface wipe, air, and dust sampling in used cars sold by non-smokers
(n = 40) and smokers (n = 87) and analyzed them for nicotine. Also, primary drivers
were interviewed about smoking behaviour [18]. The vehicle interiors were finally
inspected to investigate differences in car dustiness and signs of past smoking.
Interestingly, smokers reported using air conditioning less (p < 0.05) and driving with
windows down more often than non-smokers (p = 0.05) [18]. Also their cars were
also dustier (p < 0.01) and exhibited more ash and burn marks than non-smokers'
cars (p < 0.001). On further analysis, the number of cigarettes smoked by the primary
driver was the strongest predictor of residual TSP indicators (R(2) = .10 - .16, p =
0.001) [18]. Also, this relationship was neither mediated by ash or burn marks nor
moderated by efforts to remove residual TSP from the vehicle (i.e., cleaning,
ventilation) or attempts to prevent tobacco smoke pollutants from adsorbing while

smoking (e.g., holding the cigarette near/outside window) [18]. Two years before, the
same group developed and compared methods to measure residual contamination of

13
cars with second-hand smoke in used cars sold by non-smokers (n = 20) and
smokers (n = 87) [19]. The sellers were interviewed about smoking behaviour and
restrictions, and car interiors were inspected for signs of tobacco use. It was found
that the cars of smokers who smoked in their vehicles showed significantly elevated
levels of nicotine (p < 0.001) in dust, on surfaces, and in the air compared with non-
smoker cars with smoking ban [19]. Also, smoking more cigarettes in the car and
overall higher smoking rate of the seller were significantly associated with higher
second-hand smoke contamination of the car (p < 0.001) [19]. Interestingly, the use
of a cut point for nicotine levels from surface wipe samples correctly identified 82% of
smoker cars without smoking bans, 75% of smoker cars with bans, and 100% of non-
smoker cars [19]. Thus, it can be concluded that surface nicotine levels provide a
relatively inexpensive and accurate method to identify cars and other indoor
environments contaminated with residual second-hand smoke [19].

Conclusion
The quality of the car indoor air may be improved by procedures such as window-
opening or the correct use of fans or automated air conditioning systems (Fig. 2). In
striking contrast to the multitude of studies that address outdoor air pollution, only
little is known about indoor air quality in cars. Therefore, modern scientometric tools
which are in use for the analysis of other research are not applicable in this area [20-
32].
There are numerous approaches present which may bring light to this field of
environmental sciences. In specifics, sources and levels of different substances need
to be identified and analyzed. Then, further research should be performed about

14

mechanisms, i.e. with the use of modern techniques of biochemistry [33-36],
toxicology [37, 38] and molecular biology [39-43].

Acknowledgement
We thank G. Volante for expert help. Publication of this review was partly supported
by EUGT e. V.
Competing interests
The authors declare that they have no competing interests.
Authors' contributions
DM, DK, SU,

DAG have made substantial contributions to the conception and design
of the review, acquisition of the review data and have been involved in drafting and
revising the manuscript. All authors have read and approved the final manuscript.

15
Figure Legends

Figure 1 Factors that can influence indoor air quality in cars negatively.

Figure 2 Factors that may improve indoor air quality in cars when used correctly.

16
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proliferation and inflammation. J Pharmacol Exp Ther 2003, 304:22-29.
34. Groneberg DA, Bester C, Grutzkau A, Serowka F, Fischer A, Henz BM,
Welker P: Mast cells and vasculature in atopic dermatitis potential
stimulus of neoangiogenesis. Allergy 2005, 60:90-97.
35. Peiser C, Springer J, Groneberg DA, McGregor GP, Fischer A, Lang RE:
Leptin receptor expression in nodose ganglion cells projecting to the rat
gastric fundus. Neurosci Lett 2002, 320:41-44.
36. Groneberg DA, Peiser C, Dinh QT, Matthias J, Eynott PR, Heppt W, Carlstedt
I, Witt C, Fischer A, Chung KF: Distribution of respiratory mucin proteins
in human nasal mucosa. Laryngoscope 2003, 113:520-524.
37. Groneberg DA, Grosse-Siestrup C, Fischer A: In vitro models to study
hepatotoxicity. Toxicol Pathol 2002, 30:394-399.
38. Eynott PR, Groneberg DA, Caramori G, Adcock IM, Donnelly LE, Kharitonov

S, Barnes PJ, Chung KF: Role of nitric oxide in allergic inflammation and
bronchial hyperresponsiveness. Eur J Pharmacol 2002, 452:123-133.
39. Groneberg DA, Doring F, Nickolaus M, Daniel H, Fischer A: Expression of
PEPT2 peptide transporter mRNA and protein in glial cells of rat dorsal
root ganglia. Neurosci Lett 2001, 304:181-184.
40. Dinh QT, Groneberg DA, Peiser C, Mingomataj E, Joachim RA, Witt C, Arck
PC, Klapp BF, Fischer A: Substance P expression in TRPV1 and trkA-
positive dorsal root ganglion neurons innervating the mouse lung. Respir
Physiol Neurobiol 2004, 144:15-24.
41. Lauenstein HD, Quarcoo D, Plappert L, Schleh C, Nassimi M, Pilzner C,
Rochlitzer S, Brabet P, Welte T, Hoymann HG, et al: Pituitary adenylate

21
cyclase-activating peptide receptor 1 mediates anti-inflammatory effects
in allergic airway inflammation in mice. Clin Exp Allergy 2011, 41:592-601.
42. Dinh QT, Groneberg DA, Peiser C, Springer J, Joachim RA, Arck PC, Klapp
BF, Fischer A: Nerve growth factor-induced substance P in capsaicin-
insensitive vagal neurons innervating the lower mouse airway. Clin Exp
Allergy 2004, 34:1474-1479.
43. Groneberg DA, Fischer A, Chung KF, Daniel H: Molecular mechanisms of
pulmonary peptidomimetic drug and peptide transport. Am J Respir Cell
Mol Biol 2004, 30:251-260.


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